tbuckley/cabot-search huggingface dataset:
Reanalysis of exome negative patients with rare disease: a pragmatic workflow for diagnostic applications
Authors: Gaby Schobers, Jolanda H. Schieving, Helger G. Yntema, Maartje Pennings, Rolph Pfundt, Ronny Derks, Tom Hofste, Ilse de Wijs, Nienke Wieskamp, Simone van den Heuvel, Jordi Corominas Galbany, Christian Gilissen, Marcel Nelen, Han G. Brunner, Tjitske Kleefstra, Erik-Jan Kamsteeg, Michèl A. A. P. Willemsen, Lisenka E. L. M. Vissers
Journal: Genome Medicine (2022)

Approximately two third of patients with a rare genetic disease remain undiagnosed after exome sequencing (ES). As part of our post-test counseling procedures, patients without a conclusive diagnosis are advised to recontact their referring clinician to discuss new diagnostic opportunities in due time. We performed a systematic study of genetically undiagnosed patients 5 years after their initial negative ES report to determine the efficiency of diverse reanalysis strategies.We revisited a cohort of 150 pediatric neurology patients originally enrolled at Radboud University Medical Center, of whom 103 initially remained genetically undiagnosed. We monitored uptake of physician-initiated routine clinical and/or genetic re-evaluation (ad hoc re-evaluation) and performed systematic reanalysis, including ES-based resequencing, of all genetically undiagnosed patients (systematic re-evaluation).Ad hoc re-evaluation was initiated for 45 of 103 patients and yielded 18 diagnoses (including 1 non-genetic). Subsequent systematic re-evaluation identified another 14 diagnoses, increasing the diagnostic yield in our cohort from 31% (47/150) to 53% (79/150). New genetic diagnoses were established by reclassification of previously identified variants (10%, 3/31), reanalysis with enhanced bioinformatic pipelines (19%, 6/31), improved coverage after resequencing (29%, 9/31), and new disease-gene associations (42%, 13/31). Crucially, our systematic study also showed that 11 of the 14 further conclusive genetic diagnoses were made in patients without a genetic diagnosis that did not recontact their referring clinician.We find that upon re-evaluation of undiagnosed patients, both reanalysis of existing ES data as well as resequencing strategies are needed to identify additional genetic diagnoses. Importantly, not all patients are routinely re-evaluated in clinical care, prolonging their diagnostic trajectory, unless systematic reanalysis is facilitated. We have translated our observations into considerations for systematic and ad hoc reanalysis in routine genetic care.
Highlights From the 2022 Annual Meeting of the American Society of Clinical Oncology—Disparities in Clinical Trials, Mitigating Clinician Burnout, and Combination Treatments for Cancer
Authors: Melissa Suran
Journal: JAMA (2022)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Journals JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Two Distinct Immune Cell Signatures Predict the Clinical Outcomes in Patients With Amyopathic Dermatomyositis With Interstitial Lung Disease
Authors: Yan Ye, Xueliang Zhang, Teng Li, Jiaqiang Ma, Ran Wang, Chunmei Wu, Runci Wang, Chunde Bao, Shuang Ye, Nan Shen, Qiang Guo, Qiong Fu, Xiaoming Zhang
Journal: Arthritis & Rheumatology (2022)

Objective Amyopathic dermatomyositis (ADM) is a heterogeneous and life‐threatening autoimmune disease with a high mortality rate. In particular, anti–melanoma differentiation–associated protein 5 antibody–positive patients are at a high risk of developing rapidly progressive interstitial lung disease (RPILD). This study was undertaken to identify immunologic signatures among patients who have ADM with ILD (ADM‐ILD) and to discover the biomarkers predicting prognosis. Methods The landscape of 42 immune cell phenotypes in the peripheral blood of 82 ADM‐ILD patients and 82 age‐ and sex‐matched healthy donors was assessed by multicolor flow cytometry. Patients were stratified using an unsupervised machine learning method (hierarchical clustering analysis) by immune cell subsets. Multiple Wilcoxon's signed rank tests and supervised machine learning methods were performed to identify important immune cell subsets. Kaplan‐Meier survival analysis with log rank tests was used to create survival curves. Results We identified 2 distinct clusters correlating with different disease activities and clinical outcomes in ADM‐ILD. Cluster 1 was enriched in the activated CD45RA+HLA–DR+CD8+ T cells with decreased CD56 dim natural killer cell proportions and showed a higher prevalence of RPILD and higher mortality. In contrast, the other subgroup, cluster 2 (the nonactivated T cell–dominant cluster), displayed favorable clinical outcomes with high survival rates. Our data also revealed that immunophenotype was an independent risk factor associated with 1‐year survival. Conclusion Peripheral immunologic features may have the potential to stratify patients with ADM‐ILD according to different disease severity and clinical outcomes, which may have implications for outcome prediction, pathogenesis study, and therapy selection.
Transcriptional Plasticity Drives Leukemia Immune Escape
Authors: Kenneth Eagle, Taku Harada, Jérémie Kalfon, Monika W. Perez, Yaser Heshmati, Jazmin Ewers, Jošt Vrabič Koren, Joshua M. Dempster, Guillaume Kugener, Vikram R. Paralkar, Charles Y. Lin, Neekesh V. Dharia, Kimberly Stegmaier, Stuart H. Orkin, Maxim Pimkin
Journal: Blood Cancer Discovery (2022)

Abstract Relapse of acute myeloid leukemia (AML) after allogeneic bone marrow transplantation has been linked to immune evasion due to reduced expression of major histocompatibility complex class II (MHCII) genes through unknown mechanisms. In this work, we developed CORENODE, a computational algorithm for genome-wide transcription network decomposition that identified a transcription factor (TF) tetrad consisting of IRF8, MYB, MEF2C, and MEIS1, regulating MHCII expression in AML cells. We show that reduced MHCII expression at relapse is transcriptionally driven by combinatorial changes in the expression of these TFs, where MYB and IRF8 play major opposing roles, acting independently of the IFNγ/CIITA pathway. Beyond the MHCII genes, MYB and IRF8 antagonistically regulate a broad genetic program responsible for cytokine signaling and T-cell stimulation that displays reduced expression at relapse. A small number of cells with altered TF abundance and silenced MHCII expression are present at the time of initial leukemia diagnosis, likely contributing to eventual relapse. Significance: Our findings point to an adaptive transcriptional mechanism of AML evolution after allogeneic transplantation whereby combinatorial fluctuations of TF expression under immune pressure result in the selection of cells with a silenced T-cell stimulation program. This article is highlighted in the In This Issue feature, p. 369
Intravenous Fluids in Septic Shock — More or Less?
Authors: Lauralyn A. McIntyre, John C. Marshall
Journal: New England Journal of Medicine (2022)

…soon the sharpened features, and sunken eye, and fallen jaw, pale and cold, bearing the manifest impress of death's signet, began to glow with returning animation…. During the British cholera epidemic of 1831, William O'Shaughnessy reported that the blood of victims "has lost a large portion of its water…a great proportion of its neutral saline ingredients" and that "of the free alkali contained in healthy serum, not a particle is present in some cholera cases."1 He advocated for the restoration of the missing water and salts, an approach that was embraced by the Scottish general practitioner Thomas Latta, who reported . . .
Early changes in estimated glomerular filtration rate post‐initiation of empagliflozin in <scp>EMPEROR‐Reduced</scp>
Authors: Faiez Zannad, João Pedro Ferreira, John Gregson, Bettina Johanna Kraus, Michaela Mattheus, Sibylle Jenny Hauske, Javed Butler, Gerasimos Filippatos, Christoph Wanner, Stefan D. Anker, Stuart J. Pocock, Milton Packer
Journal: European Journal of Heart Failure (2022)
Influence of hepatotropic and metabiotic correction on the spectrum of free fatty acids in experimental toxic liver damage
Authors: V.I. Didenko, V.A. Karachynova, I.A. Klenina, Yu.А. Gaidar, N.Yu. Oshmianska, O.I. Hrabovska, O.О. Halinskyi, N.S. Vishnarevskaya
Journal: GASTROENTEROLOGY (2022)

Background. Today most of the scientists are studying the processes of hepatocyte damage under the influence of free fatty acids (FFA) in vitro conditions. Therefore, in vivo studies of the spectrum of FFA in liver pathologies of different genesis, including toxic ones, are of considerable interest. Materials and methods. Toxic liver damage was simulated by subcutaneous injection of CCl4 solution in olive oil into rats. The following groups were formed: control (healthy; n=15); I— CCl4-induced liver damage without drug correction (n=6); III— CCl4-induced liver damage + metadoxin (Liveria IC; n=8); III— CCl4-induced liver damage + metabiotic (Hilac forte) (n=7). For morphological assessment of steatosis and fibrosis we used three-color qualitative staining of liver samples by Mallory-Slinchenko. Quantitative content of monounsaturated fatty acids (MUFA) in liver homogenate was determined by gas chromatography. Results. Evaluation of hepatobioptates in group I rats revealed tissue disorganization with macrovesicular steatosis in the cytoplasm of hepatocytes, the formation of interparticle multiple fibrous septa and inflammatory cell infiltration. The use of metadoxin (group II) and metabiotic (group III) improved the morphological picture of the liver, which was damaged by CCl4. Total MUFA content increased significantly in 118 (p&lt;0.001), 34 (p&lt;0.001) and 99 times (p&lt;0.001), respectively, for groups I–III animals relative to control, but in group II— tended to decrease in 3.5 (p=0.430) and 2.9 times (p=0.064), compared to groups I and III, respectively. Conclusions. It was found that correction with methadoxin and metabioticreduced the manifestations of protein-fatty dystrophy in hepatocytes. In all animal research groups, the content of PUFA increased mainly due to significant concentrations of cis-10-pentadecenoic, cis-10-heptadecenoic, trans- and cis-9-octadecenoic and cis-11-eicosenoic acids. MUFA content decreased more under the influence of methadoxin than metabiotic.
The Nitrogen Mustards
Authors: Martin S. Highley, Bart Landuyt, Hans Prenen, Peter G. Harper, Ernst A. De Bruijn
Journal: Pharmacological Reviews (2022)

The nitrogen mustards are powerful cytotoxic and lymphoablative agents and have been used for more than 60 years. They are employed in the treatment of cancers, sarcomas, and hematologic malignancies. Cyclophosphamide, the most versatile of the nitrogen mustards, also has a place in stem cell transplantation and the therapy of autoimmune diseases. Adverse effects caused by the nitrogen mustards on the central nervous system, kidney, heart, bladder, and gonads remain important issues. Advances in analytical techniques have facilitated the investigation of the pharmacokinetics of the nitrogen mustards, especially the oxazaphosphorines, which are prodrugs requiring metabolic activation. Enzymes involved in the metabolism of cyclophosphamide and ifosfamide are very polymorphic, but a greater understanding of the pharmacogenomic influences on their activity has not yet translated into a personalized medicine approach. In addition to damaging DNA, the nitrogen mustards can act through other mechanisms, such as antiangiogenesis and immunomodulation. The immunomodulatory properties of cyclophosphamide are an area of current exploration. In particular, cyclophosphamide decreases the number and activity of regulatory T cells, and the interaction between cyclophosphamide and the intestinal microbiome is now recognized as an important factor. New derivatives of the nitrogen mustards continue to be assessed. Oxazaphosphorine analogs have been synthesized in attempts to both improve efficacy and reduce toxicity, with varying degrees of success. Combinations of the nitrogen mustards with monoclonal antibodies and small-molecule targeted agents are being evaluated. <h3>Significance Statement</h3> The nitrogen mustards are important, well-established therapeutic agents that are used to treat a variety of diseases. Their role is continuing to evolve.
Materials and extracellular matrix rigidity highlighted in tissue damages and diseases: Implication for biomaterials design and therapeutic targets
Authors: Jae Hee Park, Seung Bin Jo, Jung-Hwan Lee, Hae-Hyoung Lee, Jonathan C. Knowles, Hae-Won Kim
Journal: Bioactive Materials (2022)

Rigidity (or stiffness) of materials and extracellular matrix has proven to be one of the most significant extracellular physicochemical cues that can control diverse cell behaviors, such as contractility, motility, and spreading, and the resultant pathophysiological phenomena. Many 2D materials engineered with tunable rigidity have enabled researchers to elucidate the roles of matrix biophysical cues in diverse cellular events, including migration, lineage specification, and mechanical memory. Moreover, the recent findings accumulated under 3D environments with viscoelastic and remodeling properties pointed to the importance of dynamically changing rigidity in cell fate control, tissue repair, and disease progression. Thus, here we aim to highlight the works related with material/matrix-rigidity-mediated cell and tissue behaviors, with a brief outlook into the studies on the effects of material/matrix rigidity on cell behaviors in 2D systems, further discussion of the events and considerations in tissue-mimicking 3D conditions, and then examination of the in vivo findings that concern material/matrix rigidity. The current discussion will help understand the material/matrix-rigidity-mediated biological phenomena and further leverage the concepts to find therapeutic targets and to design implantable materials for the treatment of damaged and diseased tissues.
Cytokine release syndrome-like serum responses after COVID-19 vaccination are frequent and clinically inapparent under cancer immunotherapy
Authors: Thomas Walle, Sunanjay Bajaj, Joscha A. Kraske, Thomas Rösner, Christiane S. Cussigh, Katharina A. Kälber, Lisa Jasmin Müller, Sophia Boyoung Strobel, Jana Burghaus, Stefan M. Kallenberger, Christoph K. Stein-Thöringer, Maximilian Jenzer, Antonia Schubert, Steffen Kahle, Anja Williams, Birgit Hoyler, Lin Zielske, Renate Skatula, Stefanie Sawall, Mathias F. Leber, Russell Z. Kunes, Johannes Krisam, Carlo Fremd, Andreas Schneeweiss, Jürgen Krauss, Leonidas Apostolidis, Anne Katrin Berger, Georg M. Haag, Stefanie Zschäbitz, Niels Halama, Christoph Springfeld, Romy Kirsten, Jessica C. Hassel, Dirk Jäger, Christiane S. Cussigh, Katharina A. Kälber, Omar Abdelrahim, Elena Busch, Patrick Derigs, Katharina Dischinger, Fouad Mitri, Kerstin Schmidt, Irfan A. Bhatti, Barbara Grün, Nicolas Hohmann, Lena Woydack, Xin-Wen Zhang, Dyke Ferber, Andreas Mock, Tillmann Pompecki, Timo Schank, Carlo Fremd, Georg M. Haag, Niels Halama, Romy Kirsten, Jessica C. Hassel, Dirk Jäger, Guy Ungerechts
Journal: Nature Cancer (2022)

Patients with cancer frequently receive immune-checkpoint inhibitors (ICIs), which may modulate immune responses to COVID-19 vaccines. Recently, cytokine release syndrome (CRS) was observed in a patient with cancer who received BTN162b2 vaccination under ICI treatment. Here, we analyzed adverse events and serum cytokines in patients with 23 different tumors undergoing (n = 64) or not undergoing (n = 26) COVID-19 vaccination under ICI therapy in a prospectively planned German single-center cohort study (n = 220). We did not observe clinically relevant CRS (≥grade 2) after vaccination (95% CI 0-5.6%; Common Terminology of Adverse Events v.5.0) in this small cohort. Within 4 weeks after vaccination, serious adverse events occurred in eight patients (12.5% 95% CI 5.6-23%): six patients were hospitalized due to events common under cancer therapy including immune related adverse events and two patients died due to conditions present before vaccination. Despite absence of CRS symptoms, a set of pairwise-correlated CRS-associated cytokines, including CXCL8 and interleukin-6 was >1.5-fold upregulated in 40% (95% CI 23.9-57.9%) of patients after vaccination. Hence, elevated cytokine levels are common and not sufficient to establish CRS diagnosis.
Group Members Added to Supplement
Journal: JAMA Network Open (2022)

Virginie Lambrecq, MD, PhD; Aurélie Hanin, PharmD; Esteban Munoz-Musat, MD; Lydia Chougar, MD; Salimata Gassama, MD; Cécile Delorme, MD; Louis Cousyn, MD; Alaina Borden, MD; Maria Damiano, MD, PhD; Valerio Frazzini, MD, PhD; Gilles Huberfeld, MD, PhD; Frank Landgraf, MD; Vi-Huong Nguyen-Michel, MD; Phintip Pichit, MD; Aude Sangare, MD; Mario Chavez, PhD; Capucine Morélot-Panzini, MD, PhD; Elise Morawiec, MD; Mathieu Raux, MD, PhD; Charles-Edouard Luyt, MD, PhD; Pierre Rufat, MD; Damien Galanaud, MD, PhD; Jean-Christophe Corvol, MD, PhD; Catherine Lubetzki, MD, PhD; Benjamin Rohaut, MD, PhD; Sophie Demeret, MD; Nadya Pyatigorskaya, MD, PhD; Lionel Naccache, MD, PhD; Vincent Navarro, MD, PhD; Cohort COVID-19 Neurosciences (CoCo Neurosciences) Study Group; Jean-Yves Delattre ; Stephanie Carvalho; Sandrine Sagnes; Bruno Dubois; Celine Louapre; Tanya Stojkovic; Ahmed Idbaih; Charlotte Rosso; David Grabli; Ana Zenovia Gales; Bruno Millet; Eleonore Bayen; Sophie Dupont; Gaelle Bruneteau; Stephane Lehericy; Danielle Seilhean; Alexandra Durr; Aurelie Kas; Foudil Lamari; Marion Houot; Vanessa Batista Brochard; Pascale Pradat-Diehl; Khe Hoang-Xuan; Bertrand Fontaine; Philippe Fossati; Isabelle Arnulf; Alexandre Carpentier; Yved Edel; Anna Luisa , Di Stefano; Gilberte Robain; Philippe Thoumie; Bertrand Degos; Tarek Sharshar; Sonia Alamowitch; Emmanuelle Apartis-Bourdieu; Charles-Siegried Peretti; Renata Ursu; Nathalie Dzierzynski; Kiyoka Kinugawa Bourron; Joel Belmin; Bruno Oquendo; Eric Pautas; Marc Verny; Yves Samson; Sara Leder; Anne Leger; Sandrine Deltour; Flore Baronnet; Stéphanie Bombois; Mehdi Touat; Caroline Dehais; Caroline Houillier; Florence Laigle-Donadey; Dimitri Psimaras; Agusti Alentorn; Nadia Younan; Nicolas Villain; Maria del Mar Amador; Louise-Laure Mariani; Nicolas Mezouar; Graziella Mangone; Aurélie Meneret; Andreas Hartmann; Clément Tarrano; David Bendetowicz; Pierre-Francois Pradat; Michel Baulac; Sara Sambin; Florence Chochon; Adele Hesters; Bastien Herlin; An Hung Nguyen; Valérie Procher; Alexandre Demoule; Julien Mayaux; Morgane Faure; Claire Ewenczyk; Giulia Coarelli; Anna Heinzmann; Perrine Charles; Marion Masingue; Guillaume Bassez; Isabelle An; Yulia Worbe; Rabab Debs; Timothee Lenglet; Natalia Shor; Delphine Leclercq; Albert Cao; Clémence Marois; Nicolas Weiss; Loic Le Guennec; Vincent Degos; Alice Jacquens; Thomas Similowski; Jean-Yves Rotge; Bertrand Saudreau; Victor Pitron; Nassim Sarni; Nathalie Girault; Redwan Maatoug; Smaranda Leu; Lionel Thivart; Karima Mokhtari; Isabelle Plu; Bruno Goncalves; Laure Bottin; Marion Yger; Gaelle Ouvrard; Rebecca Haddad; Flora Ketz; Carmelo Lafuente; Christel Oasi; Bruno Megarbane; Dominique Herve; Haysam Salman; Armelle Rametti-Lacroux; Alize Chalancon; Anais Herve ; Hugo Royer; Florence Beauzor; Valentine Maheo; Christelle Laganot; Camille Minelli; Aurélie Fekete; Abel Grine; Marie Biet; Rania Hilab; Aurore Besnard; Meriem Bouguerra; Gwen Goudard; Saida Houairi; Saba Al-Youssef; Christine Pires; Anissa Oukhedouma; Katarzyna Siuda-Krzywicka; Tal Seidel Malkinson; Hanane Agguini; Hassen Douzane Agguini; Safia Said
Safety and immunogenicity of the inactivated whole-virus adjuvanted COVID-19 vaccine VLA2001: A randomized, dose escalation, double-blind phase 1/2 clinical trial in healthy adults
Authors: Rajeka Lazarus, Christian Taucher, Claire Brown, Irena Čorbic Ramljak, Leon Danon, Katrin Dubischar, Christopher J.A. Duncan, Susanne Eder-Lingelbach, Saul N. Faust, Christopher Green, Karishma Gokani, Romana Hochreiter, Johanna Kellett Wright, Dowan Kwon, Alexander Middleditch, Alasdair P.S. Munro, Kush Naker, Florentina Penciu, David Price, Benedicte Querton, Tawassal Riaz, Amy Ross-Russell, Amada Sanchez-Gonzalez, Hayley Wardle, Sarah Warren, Adam Finn
Journal: Journal of Infection (2022)
Therapeutic Targeting of Macrophage Plasticity Remodels the Tumor-Immune Microenvironment
Authors: Hee-Jin Jang, Hyun-Sung Lee, Wendong Yu, Maheshwari Ramineni, Cynthia Y. Truong, Daniela Ramos, Taylor Splawn, Jong Min Choi, Sung Yun Jung, Ju-Seog Lee, Daniel Y. Wang, Joel M. Sederstrom, Massimo Pietropaolo, Farrah Kheradmand, Christopher I. Amos, Thomas M. Wheeler, R. Taylor Ripley, Bryan M. Burt
Journal: Cancer Research (2022)

Abstract Although the majority of patients with advanced lung adenocarcinoma (LUAD) are eligible to receive immune checkpoint blockade, approximately 80% of these tumors are resistant to this therapeutic approach. Insights at the single-cell level into mechanisms that drive LUAD tumorigenesis and the relationship of LUAD histologic heterogeneity to response to immune checkpoint blockade could help identify biomarkers and potential combinational approaches to improve immunotherapy efficacy. Here, we used a genetically engineered mouse model that replicates the development of human LUAD through a spectrum of preinvasive to invasive adenocarcinoma histologic subtypes. A systems onco-immunology approach of integrating the analytical power and unique, complementary capabilities of time-of-flight mass cytometry (CyTOF) and imaging mass cytometry was leveraged to identify cellular and spatial immune contextures in LUAD. Comprehensive investigation of mouse and human LUAD using these single-cell proteomics platforms showed that LUAD progression is associated with spatiotemporal evolution of tumor-associated macrophages in the tumor-immune microenvironment, which governs tumor response to immunotherapy. PD-1 was expressed in a highly plastic tumor-promoting subtype of tumor-associated macrophages that develops during tumor progression from preinvasive to invasive adenocarcinoma, controls the lymphocyte-depleted niche of invasive tumors, and protects tumor cells in the solid histologic components of the tumor. Longitudinal, multidimensional single-cell analyses of LUAD tumorigenesis revealed dynamic alteration of immunoregulatory PD-1–expressing tumor-associated macrophages that can be targeted to overcome resistance to checkpoint immunotherapy. Significance: Comprehensive single-cell proteomics analyses of lung adenocarcinoma progression reveal the role of tumor-associated macrophages in resistance to PD-1 blockade therapy. See related commentary by Lee et al., p. 2515
Regional specification of oral mucosal immunity
Authors: Drake W. Williams, George Hajishengallis, Niki M. Moutsopoulos
Journal: Science Immunology (2022)

In this issue of Science Immunology , Barreto de Albuquerque et al. track immune responsiveness to the foodborne pathogen Listeria monocytogenes during oral infection. Their findings extend the notion of compartmentalized immunity within the gastrointestinal tract to the oral cavity and provide previously unkown insights into regional specialization of oral immunity.